Sir: I present a case of risperidone-induced tardive dyskinesia that is unusual because the patient had never been treated with the typical antipsychotics and the dose of risperidone was only 1 mg/day. During his withdrawal, symptoms fluctuated in an inverse relationship with the increase and decrease of risperidone dose. Case report. Mr. A, a 50-year-old divorced white man, has been receiving psychiatric treatment for 16 years. He suffers from recurrent major depression and was hospitalized twice in the past 5 years with suicidal ideation. In addition to various antidepressants, he was tried for short periods of time on lithium, carbamazepine, and divalproex sodium with no discernible benefit. In the spring of 1996, after unsuccessful trials of paroxetine and nefazodone, he was started on fluvoxamine 50 mg/day and risperidone 0.5 mg h.s. A month later, risperidone was increased to 1 mg h.s., and fluvoxamine was slowly increased to 200 mg/day. In the fall of 1996, because Mr. A was no better, fluvoxamine was tapered off, and he was given fluoxetine 40 mg/day with which he was treated successfully a few years earlier. Risperidone 1 mg/day was continued. In late November 1996, he showed blinking of the eyes, parkinsonian tremor of the hands, and some tongue-rolling movements. Risperidone was stopped and fluoxetine reduced to 20 mg/day. Gradually, the abnormal movements worsened, and a month later the blinking was so frequent and constant that he was not able to read, watch television, or drive his car. His respiration became labored and deep with occasional high-pitched vocal sounds during expiration. He was restarted on risperidone 0.5 mg h.s., and a month later clorazepate 15 mg/day in divided dosage was added. His symptoms improved minimally, but he developed suicidal impulses and was rehospitalized for 8 days in January 1997. His symptoms were suppressed with increased dosage of risperidone 2 mg/day and fluoxetine 40 mg/day. Another attempt was then made to withdraw risperidone. Blepharospasm and labored breathing returned. He also started to make cluck

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SynopsisEleven patients in remission from manic-depressive illness were studied by means of metabolic balances before and after the administration of lithium carbonate. Lithium caused a sharp diuresis of isotonic saline and a smaller excretion of potassium over the course of two days. During the subsequent two days there occurred a compensatory retention of Na, K and water. These short-term changes were not associated with any significant alteration in the patients' mood. There was no significant and systematic retention of Na, K or water over the 14 days of Li administration. The recovery of Li was measured simultaneously. During the first week only a proportion of the administered Li was recovered in the urine and faeces, suggesting that a gradual distribution of Li throughout its body space was occurring. After the first week, nearly all the administered Li was recovered, indicating an equilibrium with an even distribution of the ion throughout its body space. This equilibrium was more complete at this early stage in those patients who had been given a smaller dose of lithium carbonate.

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As Dr Checkley points out, a further stimulus to a continued effort to evaluate this interrelationship comes from the established knowledge that lithium, one of the most effective anti-manic agents, does have a very marked anti-thyroid effect. We have recently begun to study in a prospective longitudinal design an individual who has both rapidly cycling manic-depressive illness and also severe hypothyroidism when on lithium carbonate. The initial evidence suggests that the thyroid hormones may be capable of playing an important physiological role in the modulation of affective illness, a rising level of thyroid hormone available to the cell being adaptive and therapeutic during depression but maladaptive and capable of inducing mania when bipolar illness is also present.